Stimulation of Na+/Mg2+ antiport in rat erythrocytes by intracellular Cl−

FEBS Letters

Ebel, H.²  Günther, T.¹ 

[1] Institut für Molekularbiologie und Biochemie, Klinikum Benjamin Franklin, Freie Universität Berlin, Arnimallee 22, 14195 Berlin, Germany;Institut für Klinische Physiologie, Klinikum Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 30, 12200 Berlin, Germany

关键词: Na+/Mg2+ antiport;    [Cl−]i stimulation;    Deoxygenation;    Essential hypertension;    Rat erythrocyte;   

DOI  :  10.1016/S0014-5793(03)00417-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Mg²⁺ efflux from rat erythrocytes was measured in NaCl, NaNO₃, NaSCN and Na gluconate medium. Substitution of extracellular and intracellular Cl⁻ with the permeant anions NO₃ ⁻ and SCN⁻ reduced Mg²⁺ efflux via Na⁺/Mg²⁺ antiport. After substitution of extracellular Cl⁻ with the non-permeant anion gluconate, Mg²⁺ efflux was not significantly reduced. In Na gluconate medium, an influence of the changed membrane potential and intracellular pH on Mg²⁺ efflux could be excluded. The results indicate the existence of Cl⁻-independent Na⁺/Mg²⁺ antiport and of Na⁺/Mg²⁺ antiport stimulated by intracellular Cl⁻. Intracellular Cl⁻, as determined by means of ³⁶Cl⁻, was found to stimulate Na⁺/Mg²⁺ antiport through a cooperative effect according to a sigmoidal kinetics. The Hill coefficient for intracellular Cl⁻ amounted to 1.4–1.8, indicating that two intracellular Cl⁻ may be simultaneously active. With respect to specificity, Cl⁻ was most effective, followed by Br⁻, J⁻, and F⁻. Stimulation of Na⁺/Mg²⁺ antiport by intracellular Cl⁻ together with intracellular Mg²⁺ may play a role during deoxygenation of erythrocytes and in essential hypertension.

【 授权许可】

Unknown